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Biomedical subjects

L G Collins

Publications and source records attributed to L G Collins.

11 recordsLinked to original sources
PubMed1996

Laparoscopic extraperitoneal herniorrhaphy.

Laparoscopic extraperitoneal (LEP) herniorrhaphy procedures allow direct visualization and repair of many types of hernias (e.g., direct, indirect, femoral, sliding, bilateral). Common complications of open herniorrhaphy procedures are avoided when LEP herniorrhaphy procedures are used because the peritoneum is not entered. The placement of synthetic mesh in the preperitoneal space during LEP herniorrhaphy procedures prevents inadvertent contact with peritoneal contents and minimizes patients' risks of adhesions, bowel obstructions, fistulas, and intraabdominal vascular injuries. Improved anatomic presentation and optimal patient outcomes are achieved with this approach.

Hernia, Inguinal↗
PubMed1987

Multiple hereditary ocular anomalies in a herd of cattle.

A Brahman x Santa Gertrudis herd of cows bred to a Hereford bull was evaluated because of a 3-year history of several calves born with congenital blindness. Multiple congenital ocular anomalies in 2 calves included microphthalmos, microcornea, microcoria, heterochromia iridis, microlentia, cataracts, retinal dysplasia, retinal detachment, anterior segment dysgenesis, acorea, and proliferation of the anterior neuroectoderm. On the basis of the lack of environmental factors and persistence of an intermittent problem when breeding to a single bull, a genetic defect was diagnosed as the probable cause. Dominant inheritance with varied expressivity may have best explained the lack of obvious signs in the bull, with emergence of various anterior and posterior segment defects in offspring from unrelated cows.

Abnormalities, Multiple↗
PubMed1986

Colonic perforation in corticosteroid-treated dogs.

Clinical findings for 5 new cases of colonic perforation in corticosteroid-treated dogs were presented and 8 other cases from the literature were reviewed. Colonic perforation was a fatal complication in all 13 dogs, 12 of which had had recent major surgery. Ten dogs were neurosurgical patients, 1 dog received medical therapy for head trauma and nonambulatory paresis, and 2 dogs were operated on for non-neurologic conditions. Dexamethasone was the most frequently used corticosteroid, and 12 dogs received a mean cumulative dose of 6.4 mg/kg over an average period of 5.1 days. Depression, anorexia, and emesis, the most frequent signs attending colonic perforation, became evident 3 to 8 days after surgery. Signs preceded death by an average of 22.3 hours. Correct antemortem diagnosis (5 dogs) and surgical intervention (3 dogs) had no effect on eventual outcome (mortality = 100%). Colonic perforation most frequently developed in the proximal descending portion and always involved the antimesenteric border. Gross fecal contamination of the peritoneal cavity and acute generalized peritonitis were evident in all but one dog. Adhesions were observed at the lesion site in 6 dogs, but prevented gross soilage in only one dog.

Adrenal Cortex Hormones↗
PubMed1985

Experimentally induced phenylbutazone toxicosis in ponies: description of the syndrome and its prevention with synthetic prostaglandin E2.

Phenylbutazone (PBZ) toxicosis was induced in 9 ponies to further define the clinical and pathologic changes occurring with this syndrome. Six additional ponies were treated with PBZ and a synthetic prostaglandin E2 to determine the role of prostaglandins in the pathogenesis of PBZ toxicosis. Ponies given only PBZ exhibited CNS depression, anorexia, weight loss, diarrhea, cyanotic mucous membranes, and oral ulcers. Total serum protein concentration gradually decreased during the 10-day treatment period. Marked mucosal atrophy, focal erosions, and ulcers characterized the lesions in the alimentary tract. Ponies given PBZ and prostaglandin E2 remained clinically healthy and did not develop hypoproteinemia or mucosal atrophy. A few erosions were seen, but ulcers were not observed. The results of the present study indicate that mucosal atrophy is a characteristic lesion of PBZ toxicosis. It is also evident that inhibition of prostaglandin synthesis has an important role in the development of this syndrome.

Animals↗
PubMed1984

Phenylbutazone toxicosis in the horse: a clinical study.

In a retrospective study of 269 horses that had been treated with phenylbutazone, horses receiving less than or equal to 8.8 mg/kg of body weight/day for less than or equal to 4 days or 2 to 4 mg/kg of body weight/day for up to 50 days remained clinically normal. Anorexia, depression, colic, hypoproteinemia, diarrhea, melena, weight loss, ventral edema, petechial hemorrhages of mucous membranes, oral and gastrointestinal tract erosions and ulcers, renal papillary necrosis, and death were among the complications seen in horses that had received greater than 8.8 mg/kg of body weight/day. In 2 cases, signs suggestive of gastrointestinal-related shock were also evident.

Administration, Oral↗